RICKETTSIACEAE &

CHLAMYDIAE
 RICKETTSIACEAE
Small gram negative bacilli, non capsulated, non
motile, obligate parasites of arthropods lice, fleas
and ticks
Arthropods vector for transmission in humans
Infect vascular endothelium and reticulo
endothelium.
Rickettsiae three genera
1.Rickettsia
2.Rochelima
3.Coxiella
CULTIVATION
Unable to grow in artificial media
Grow in yolk sac of chick embryo
Grow in mouse fibroblast, HeLa, Hep-2 continuous
cell lines.
Also propagated in arthropods
ANTIGEN
Three types antigen
Group specific soluble antigen surface
Core antigen body surface
Alkali soluble polysaccharide antigen
Some share Proteus OXK & OX2 antigen used to
demonstrate presence of rickettsiae in Weil Felix
Reaction in Typhus patient
PATHOGENICITY
Typhus Fever group
Typhus cloud/smoke cloudy state of
lesion
Include epidemic typhus, recrudescent
typhus, endemic typhus.
1.Epidemic typhus:
Causative agent: Rickettsia prowazekii
Vector : human body louse
Pathogenesis
The louse acquire the pathogen during the blood meal from
rickettsemic person
Rickettsiae enter into the blood of the insect and then
multiply in large number
During the next blood meal, the louse injects the pathogen
to a healthy person
Rickettsia enter into the blood stream and infect the
endothelial cells of the blood vessel
Cause vasculitis (inflammation of
blood vessel)
Incubation period 5 -21 days
Disease starts with fever and Chill

The fifth day rash appear first in trunk spreads to limb, face,
palm & soles

The macula papular rash then becomes cloudy

2.Recrudescent Typhus
Causative agent Rickettsia typhii
3. Endemic Typhus
Causative agent Rickettsia typhii
Disease spreads thro flea from rodents
Transmits fro rat to rat
In human infection by bite of infected flea
4. Scrub Typhus
Causative agent Rickettsia tustsugamushi
(tustsuga dangerous, mushi insect/mice)
Common in Japan
Incubation period 1-3 weeks
Red macular rash eschar formation
5.Rocky mountain spotted fever
Causative agent Rickettsia rickettsi
Multiplies in nucleus and cytoplam of cell of
louse/tick
Pathogen injected to human by bite of infected
tick / lice
Produce macular rash primarily, then becomes
petechial
Rash first appear on flexer aspect of wrist and
ankle then spreads all over the body including
palms, soles and buccal mucosa
6.Rickettsial Pox
Causative agent Rickettsia akari
Self limiting non fatal disease
Scrotal swelling in guinea pigs and human
Q fever
Causative agent Coxiella burnetii. The
infection is acquired by inhalation of infectious
material (aerosoles)
After an incubation of 14-26 days there is a
sudden onset of fever, chills, and headache,
but no rash.
The disease is characteristically an atypical
pneumonia lasting 5-14 days with a low
mortality rate.
 Lab Diagnosis
Microscopy
Small, pleomorphic coccobacilli
Gram stain poorly, but appear to be G-
Stain readily with Giemsa

Diagnosis/serological tests
Direct detection of Rickettsia in tissues (Giemsa stain
or direct fluorescent antibody test) Weil-Felix reaction
in certain rickettsial infections (typhus group)
antibodies are formed that will agglutinate OX strains of
Proteus vulgaris.
Agglutination or complement fixation tests using
specific Rickettsial antigens are better serological
diagnostic tests.
Treatment/antimicrobial therapy
Chloramphenicol or tetracycline
Wear protective clothing and use insect repellents.
 CHLAMYDIAE
Chlamydiae are obligate intracellular bacterial
parasite of human beings
Affect columnar or transitional epithelial cells
of mucous membrane
Primarily called as PPLT (Psittacosis Lympho
granuloma Trachoma)
Genus Chlamydia; contain 3 species
1.Chlamydiae trachomatis
2.Chlamydiae psittaci
3.Chlamydiae pneumoniae
Diseases Trachoma, Conjuctivitis, psittacosis
and genital infections
Morphology
Occurs in 2 forms
1.Elementary body
Size 0.2m, rigid cell wall, highly infectious,
non growing forms.
2. Reticulate body
Size - 1 m, fragile cell wall, pleomorphic,
intracellular growing and reproductive , non
infectious form
Life cycle
The infectious form is called an elementary body
(EB) which is circular in form and is taken into the
cell by induced phagocytosis.
Inside the phagocytic vesicle replication takes
place
Over the next 6-8 hours,the EB re-organizes into
the non-infectious, but metabolically active
reticulate body (RB) which is larger and less dense
than the EB.
For 18-24 hours the RB synthesized new materials
and divides by binary division to form inclusion
bodies that re-organize and condense into EBs.
Between 48-72 hours, the cell lyses and releases
the EB which begin the cycle again.
Antigenic Properties
Three major ag
First heat stable genus specific
Lipopolysaccharide antigen
Second Species specific Protein antigen
Third- outer membrane protein.
Pathogenesis
1) Trachoma
Causative agent Chlamydiae trachomatis
Transmitted eye to eye by fingers, fomites, flies
transmit mechanically, infectious dust
Affect conjunctival sac. Four stages
Stage 1
Suspicious trachoma dubium, entry of parasite
into host conjuctival sac or initiated by infectious
dust
Stage 2
Conjuctival lesion Protrachoma
Stage 3 & 4
Established or Progressive trachoma
Enlargement sac lead to
follicular hypertrophy
Superficial vascularization of cornea with
infilteration of granulated tissue producing
pannus.
2)Inclusion Conjuctivitis
Causative agent C.trachomatis type D-K
1.Neonatal form of Inclusion conjuctivitis Inclusion
blenorrhea
The infant gets infection from mother during birth from birth
passage
Visible only after 5-10 days of birth
Self limiting disease, prevented by local application of
tetracycline
2.In adults , transmitted by swimming pool water-
Swimming pol Conjuctivitis.
Pool water contaminated by genital secretion of infected
bather
Susceptible person gets infection during swimming
Produces follicular hypertrophy with scanty non purulent
discharge
3)Infant Pneumoniae
Causative agent Chlamydiae trachomatis
Infects infants of 4-16 weeks old
Symptoms cough and wheezing, rarely
accompanied by fever.
Toxicity minimal
4)Genital Infection Two types of infection
1.Genital chlamydiasis
Causative agent Chlamydiae trachomatis
oxalogenetis serotype D-K
Cause infection similar to gonococci, both infection
may coexist
In man, Inflammation of urethra urethritis
Elongated cord like structure along posterior border
of testis Epididymitis
Woman inflammation of uterine tube Salpingitis,
endometritis and mucopurulent cervicitis.
5)Lymphogranuloma venereum
Causative agent Chlamydiae trachomatis serovar L1,
L2, L3 and LGV
Disease tropical bubo(bubo enlarged lymphnode)
Pathogen multiply in regional lymphnode
Produce primary lesion small papulo vesicular lesion
on external genitalia
Incubation period 3-5 weeks
Two weeks later Secondary infection
Man infect inguinal lymphnode, Women intrapelvic /
pararectal node
Node enlarge, suppurate ,breakdown and form Sinus,
Discharge Pus and lesion spread to joint, eyes and
meninges.
Tertiary chronic, lasts for years pathogen produce
scars lymphatic blockage, woman elephantiasis of
vulva
6)Psittacosis
Causative agent Chlamydiae psittaci
Disease of parrots and birds
Spread from birds to human beings
Incubation period 10 days
Birds Diarrhea, septicemia, endocarditis and
meningo encephalitis
Lab Diagnosis
A Giemsa stain can be used to visualize
chlamydial inclusions in tissues.
Elementery bodies light microscope
Identification
Direct methods stain tissues with Giemsa or
use a direct fluorescent antibody technique.
The most sensitive method is to culture the
organisms in tissue cultures and then stain
the infected tissue culture cells
ELISA for detection of antigens
Chlamydia in
tissues
Chlamydia inclusion
bodies
Treatment
Local application and oral administartion of
sulphonamides and tetracycline
Vaccination not effective